All these changes and a series of PCOS traits, including polycystic ovarian morphology and ovulation disorders, were rescued after treatment with the ferroptosis inhibitor Fer-1 in the rat model; the mechanism of which is that DHT induces NCOA4-dependent ferritinophagy and GPX4 loss, leading to the ferroptosis in GCs (Figs 6 and 8). The gene discussed is GPX4; the disease is polycystic ovary syndrome.